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The Effect of the Level of Sex Hormones in the Prenatal Environment and its Effect on Later Sexual Development

DagherM By DagherM Published on March 18, 2016

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Today, more research is being done on sexual development than ever before. This is not surprising if you think about how important the topic is and how crucial its implications are on many different dimensions of our lives. The more this area has been explored, the more intricate and complex it proves to be. There is a growing body of research suggesting that the prenatal environment in which the fetus develops has a great impact on later sexual development. Even the smallest change in the levels of sex hormones can have a huge effect on an individual. Most scientists agree that there are many factors that can induce a change in the prenatal environment significant enough to permanently alter the course of the individual’s development. Generally speaking, there are three major areas of sexual development that can be affected: physiology, endocrinology, and behaviour.

Let us start by examining the ways in which the natural balance of hormones in the prenatal environment can be disrupted. There are three major factors that contribute to such fluctuations. First is the exposure of the fetus to certain chemical compounds through the mother’s blood stream (Meijer et al., 2012). These chemicals either alter the rate of production of specific fetal sex hormones or prevent the fetus from properly using them. The second major cause is prenatal stress. Stress can often disrupt the surge of androgens, mainly testosterone, which is essential for normal male development (Hines, 2011). The third major cause is an autosomal recessive genetic disorder known as congenital adrenal hyperplasia (CAH). CAH is caused by a deficiency in an enzyme that results in an overproduction of, and hence an overexposure to, testosterone in utero (Nimkarn & New, 2010).

The effects of a prenatal hormonal imbalance are widespread but the physiological effects are perhaps the most understood. This is mainly due to the fact that physical changes are easy to identify and measure. Therefore, we begin our discussion about the impact of hormonal imbalances by examining the physiological effects. In a study by Meijer et al. (2012), the influence of prenatal exposure to organohalogenic compounds (OHCs) and brominated flame retardants (BFRs) on sex hormone level, testes volume and penile length was examined. OHCs and BFRs are chemical compounds found in a variety of plastics, chemical solvents, and even some medicines such as Prozac. They found a high correlation between BFR exposure and increased testes volume by the age of eighteen months. Increased testes volume at this age is linked with low sperm production later on in life and an increased risk of testicular cancer. Contrary to the initial hypotheses, no connection was found between OHC/BFR exposure and penile length. Another study suggests that there is a negative correlation between the mother’s exposure to pesticides during pregnancy and her son’s testes volume and penile length at birth (Andersen et al., 2008). Although these two studies offer slightly different results, they both highlight an irrefutable finding: exposure to certain chemical compounds prenatally can substantially affect physical sexual development.

A second form of genital malformation is observed in individuals with CAH. According to the Mayo Clinic website, males who are affected by CAH develop abnormally large genitals whereas females develop genitals that are ambiguous and atypical in appearance (for example, a severely enlarged clitoris). In some extreme cases, CAH disfigures the female external genitalia to such a degree that the newborn is mistakenly thought to be male.

The third physiological change has nothing to do with genitals but with the structure of the brain. Scientists have identified a cluster of cells on the hypothalamus which plays a major role in individual’s sex drives and partner preference (which will be discussed later). This cluster is referred to as the sexually dimorphic nucleus (SDN) and is usually twice as large in males as it is in females. However, by exposing a female to higher levels of testosterone and lower levels of estrogen, the size of the SDN can be increased until it is identical to that of a normal male and vice versa (LeVay, 2011). This yet again illustrates how the physical aspect of sexual development is greatly affected by prenatal hormonal levels.

From the physiological effects, we now move to the endocrinological effects. The first is an imbalance in the serum levels of sex hormones in newborns which is caused by the exposure of the mother to certain chemicals during pregnancy. In the study previously mentioned, Meijer et al. (2012) concluded that exposing the fetus to high levels of OHCs and BFRs had a great impact on the serum levels of sex hormones in a sample of three-month-old infants.

Second, there is evidence that the amount of testosterone that individual females produce has a genetic basis and is inherited from the mother. The higher the levels of testosterone the mother produces, and consequently the more testosterone her fetus is exposed to in utero, the higher the level of testosterone her daughters will produce. No such relationship has been reported in males (Hines, 2011).

The third effect is fully dependant on the mother herself and, more importantly, how many previous sons she has borne. When a mother is pregnant with her first son, her body is being exposed to male hormones and substances for the first time. Her body eventually forms antibodies against these male-exclusive substances. When she becomes pregnant with her second son, these antibodies will enter the son’s bloodstream through the placenta, altering sexually dimorphic brain structures and decreasing the level of androgens his body can produce and use. The effect is multiplied with each new male fetus. This phenomenon is only applicable to males and is generally referred to as the fraternal birth order (FBO) effect. Many people believe that the FBO effect may be the cause for homosexuality (Bogaert & Skorska, 2011). Since androgens are responsible for attraction to females (Berenbaum & Beltz, 2011), the lowered exposure to androgens coupled with the altered SDN (which is responsible for sex drives and partner preference) could provide a biological explanation for homosexuality.

It is important to mention here that, contrary to popular belief, endocrinology has little to do with gender identity. Natural experiments suggest that levels of androgens, or lack thereof, are not what make an individual identify his/herself as male or female. Instead sexual identity has been shown to be more greatly influenced by the physical appearance of the genitals and how the individuals were reared. More research needs to be done on this subject before any final conclusions are made but preliminary studies have shown that high prenatal androgen exposure makes it more likely that an individual will come to identify him/herself as male (Berenbaum & Beltz, 2011).

It is also important to keep in mind that physiology and endocrinology are in constant interplay. In most cases, there is no way to assert any causal relationship. Often it is not clear whether an improperly developed gland has led to an imbalance in bodily hormones or if an imbalance in hormones has led to the underdevelopment of a gland. Even though the cause can be easily separated from the effect in some cases, the relationship is generally considered to be bidirectional.

Behaviour is probably the most affected area of development. From how aggressive an individual is to what kind of toys he/she likes to play with, the effects of prenatal hormones on behaviour are manifold. To study behaviour, scientists have observed gender related behaviour: the behaviour, interests, and preferences that differ between males and females in a certain cultural context (Meyer-Bahlburg et al., 2003).

Nowhere are these gender related differences displayed more prominently than in early and middle childhood. For example, boys prefer toys that are vehicles and action figures whereas girls tend to prefer toys such as tea sets and dolls. Another notable difference is that, at this age, children play mainly with same sexed children. Also, the quality of play differs greatly between genders. Boys are usually more physical in their play, engaging in more “rough and tumble play” with increased bodily contact. This is a distinction that can be observed in almost all species of mammals. Finally, males tend to be more aggressive and competitive as opposed to females who are more reserved and cooperation-focused (Hines, 2011).

Psychologists have been trying to determine the cause of these gender behaviour differences. They have concluded that it is due to the interplay of both biological factors and early socialization. One example of a biological factor that can affect gender behaviour differences is exposure to hormones in utero. Studies have shown that androgens play a big role in developing male patterns of behaviour and preferences. When males are exposed to less androgens in the mother’s womb, they display less male type behaviour. They prefer female type play, have female peer groups, and show decreased aggression. By the same token, when females are exposed to high levels of androgens in the womb, they display highly masculine patterns of behaviour and preferences in play and aggression (Hines, 2011).

Very interestingly, there is also evidence that the hormone levels in the prenatal environment play a role in masculinising or feminising the brain and individual cognitive abilities. Similar to behaviour, there are gender related differences in cognitive abilities. This is not to say that males and females differ in overall cognitive ability, but there are documented differences in the pattern of cognitive function between the sexes. Men normally outperform women in tasks that involve spatial relations and perceptions such as mentally rotating a three dimensional object. Women outperform men when it comes to task involving verbal skills such as reading comprehension and phonological processing. However, both male and female fetuses exposed to imbalanced levels of hormones during gestation display cognitive abilities that are atypical for their respective genders. Females exposed to high levels of androgens display a higher proficiency in spatial relation and a lower proficiency in verbal skills than standard females, and males who were exposed to less androgens lose their edge in spatial relations but have a better grasp of verbal skills than other males (Berenbaum & Beltz, 2011).

There is some recent evidence suggesting that this change in cognitive skills may, in some cases, result in learning disorders. In one study, Inozemtseva, Matute and Juárez (2008) examined the relationship between females with CAH, learning disabilities and sexually dimorphic abilities. Inozemtseva et al. (2008) found evidence that females who had been affected by CAH had a higher rate of learning disorders than unaffected females. Most of the learning disorders were reading disabilities. This makes sense since, as mentioned before, exposure to high levels of androgens in utero has been shown to decrease verbal skills. However, these results should be interpreted cautiously due to the fact that the sample was not representative and the fact that the CAH sample was more varied than the comparison sample (Berenbaum & Beltz, 2011). More research is warranted in this field to see if there really is a relationship between prenatal androgen exposure and learning disabilities.

In conclusion, it would be safe to say that a big part of who we are, how we see ourselves, and how we act is dictated by the prenatal environment that we developed in. The impact of the few months we spend in the womb is proof that development is truly cumulative and delicate. Chemical compounds, stress, and genetic disorders such as CAH can induce a change in the sex hormone levels of the prenatal environment. Due to this subtle change, some areas of future development are affected. These effects can generally be categorized into physiological, endocrinological, and behavioural. The prenatal environment affects everything from what toys we play with to how efficient we are in tasks of spatial relations and, as recent research suggests, may even play a role in determining learning disabilities. Further research in this field will help us explain behaviour and may even allow us to intervene in the fetal development to avoid unwanted behaviours, physiology and endocrinology. The ability to do so would present many opportunities to prevent individuals from having to go through the complicated effects of a prenatal imbalance in sex hormones.


Congenital Adrenal Hyperplasia. (n. d.). In Mayo Clinic. Retrieved from http://www.mayoclinic.com/health/congenital-adrenal-hyperplasia/DS00915/

Berenbaum, S. A. & Beltz, A. M. (2011). Sexual differentiation of human behavior: Effects of prenatal and pubertal organizational hormones. Frontiers in Neuroendocrinology, 32(2), 183-200. doi: 10.1016/j.yfrne.2011.03.001

Bogaert, A. F., & Skorska, M. (2011). Sexual orientation, fraternal birth order, and the maternal immune hypothesis: A review. Frontiers in Neuroendocrinology, 32(2), 247-254. doi: 10.1016/j.yfrne.2011.02.004

Inozemtseva, O., Matute, E., & Juárez, J. (2008). Learning Disabilities Spectrum and Sexual Dimorphic Abilities in Girls with Congenital Adrenal Hyperplasia. Journal Of Child Neurology, 23(8), 862-869. doi: 10.1177/0883073808315618

LeVay, S. (2011). From mice to men: Biological factors in the development of sexuality. Frontiers in Neuroendocrinology, 32(2), 110-113. doi: 10.1016/j.yfrne.2011.02.002

Meijer, L., Martijn, A., Melessen, J., Brouwer, A., Weiss, J., de Jong, F.H., & Sauer, P.J.J. (2012). Influence of prenatal organohalogen levels on infant male sexual development: Sex hormone levels, testes volume and penile length. Human Reproduction, 27(3), 867–872. doi: 10.1093/humrep/der426

Melissa, H. (2011). Prenatal endocrine influences on sexual orientation and on sexually differentiated childhood behavior. Frontiers in Neuroendocrinology, 32(2), 170-182. doi: 10.1016/j.yfrne.2011.02.006

Meyer-Bahlburg, H. F. L., Dolezal, C., Baker, S. W., Carlson, A. D., Obeid, J. S., & New, M. I. (2004). Prenatal androgenization affect gender-related behavior but not gender identity in 5–12-year-old girls with congenital adrenal hyperplasia. Archives of Sexual Behavior, 33(2), 97–104.

Nimkarn, S., & New, M. L. (2010). Congenital adrenal hyperplasia due to 21-hydroxylase deficiency: A paradigm for prenatal diagnosis and treatment. Annals of the New York Academy of Sciences, 1192, 5-11. doi: 10.1111/j.1749-6632.2009.05225.x

Psychology graduate currently pursuing a medical degree.

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